Cadmium poisoning is a combination of toxic effects that develop in response to the accumulation of high concentrations of metal in the body. Symptoms depend on the way cadmium enters the body. When inhaling toxic fumes, shortness of breath, cough, cyanosis, pulmonary edema develops. When penetrating through the gastrointestinal tract, diarrhea and vomiting occur. Chronic intoxication causes kidney damage, osteomalacia, pneumofibrosis. Clinical and anamnestic data, determination of metal in biomaterial, examination of biopsies are used in diagnostics. Help with poisoning includes detoxification, maintenance of breathing, cardiac activity, renal function.
T56.3 Toxic effect of cadmium and its compounds
Cadmium (Cd) is not an essential trace element, in toxicology it refers to substances with a high ability to accumulate in the body. Cadmium is practically absent in the tissues of newborns, but by the age of 50 its total content in the body can reach 20-30 mg. Excess cadmium causes acute poisoning or chronic intoxication. An example of chronic cadmium is the outbreak of Itai-itai disease that swept the Japanese prefecture of Toyama in 1950. Widespread contamination of soils, water and air with toxicants, including cadmium, dictates increased vigilance against possible mass poisoning.
There are two possible ways of penetration of the toxicant – food and inhalation. Cadmium can enter the body through the gastrointestinal tract (with food and drinking water), the respiratory system (with atmospheric air and cigarette smoke). On average, 10-40 micrograms of cadmium are supplied with food per day, 2-5 micrograms with water, 0.1–0.8 micrograms with inhaled air. At the same time, the optimal daily dose is less than 5 micrograms, toxic – 3-330 mg, lethal – more than 1.5 g. The main causes of cadmium poisoning are:
- Soil and water pollution. The danger is the consumption of food crops grown on soils with a high content of cadmium, as well as drinking contaminated water. Cadmium can intensively accumulate marine mollusks (oysters, mussels), leafy vegetables (lettuce, spinach, cabbage, sorrel), cereals (rice), mushrooms, liver and kidneys of farm animals.
- Tobacco smoking. The cause of intoxication can be active smoking in adults and passive smoking in children. When smoking one pack of tobacco products, 20 micrograms of cadmium is additionally adsorbed in the lungs. In the lungs of a smoker, the concentration of Cd is 7.5 times higher than in non-smokers.
- Professional contact with cadmium. The risk of intoxication is significantly increased among workers of ore deposits (for the extraction of zinc, lead, copper), paint and varnish industries, electrical, chemical, metallurgical industries, landfills. Also, the risk group for acute poisoning with cadmium oxide vapors (CdO) includes welders, jewelers, and soldering irons.
With food, about 80% of cadmium enters the body through the gastrointestinal tract, the remaining 20% is inhaled by a person with air and tobacco smoke. At the same time, about 5% of the toxicant is absorbed in the small intestine, and up to 50% in the respiratory tract. The lack of other trace elements (calcium, zinc, selenium, copper, iron), fiber, pectin significantly increases Cd adsorption. In the body, cadmium is deposited mainly in the kidneys and liver, in smaller quantities – in the spleen, pancreas, bone tissue. Excretion is extremely slow (0.01% per day).
The physiological significance of Cd has been little studied. It is known that together with other metals it activates a number of enzymes: tryptophan dioxygenase, DALA dehydratase, carboxypeptidase. In tissues and organs, the trace element is present in a free or bound form – in the structure of the metallothionein protein, which promotes the excretion of heavy metals. By its effect on the body, cadmium refers to thiol poisons that block the proteins of the sulfhydryl group and disrupt metabolic processes.
The nephrotoxicity of cadmium is manifested by its ability to initiate the development of renal tubular acidosis, block the reabsorption of calcium and, as a consequence, lead to calcipenic and phosphopenic variants of osteomalacia. The pneumotoxic effect is realized due to the destruction of the epithelium of the upper respiratory tract, accumulation in the lung tissue with the development of pneumofibrosis and emphysema.
Cadmium can cause changes in vascular endothelium, accumulation of lipids in vascular walls, oxidative stress, inflammatory processes (vasculitis). With prolonged exposure to Cd, toxic damage to cardiomyocytes occurs, dilation of the heart chambers. Carcinogenic, immunotoxic, neurotoxic, mutagenic effects of cadmium are also described.
With the simultaneous use of toxic doses of cadmium with food, there are signs of food poisoning by the type of gastroenteritis with vomiting, diarrhea. Hypersalivation, spastic pain in the epigastrium and right hypochondrium are possible.
Inhalation of cadmium-containing vapors or dust is more dangerous. With inhalation poisoning, signs of nasopharyngeal irritation and sore throat appear at first. Develops weakness, headache, chills. Chest pain, cough, difficulty breathing, cyanosis, tachycardia are added. Acute poisoning can lead to tracheobronchitis, bronchiolitis, bronchopneumonia, pulmonary edema.
Chronic poisoning with cadmium salts was first recorded in Japan in the middle of the twentieth century as a result of contamination of reservoirs with heavy metals during ore mining. Subsequently, these water sources were used by the local population for irrigation of fields and fishing, and the resulting products (rice, soy, fish) were consumed for a long time.
The disease was named “itai-itai”, which means “it hurts-it hurts”. Residents of the area where chronic cadmium was recorded complained of unbearable pain in the joints, bones, and lower back. As a result of osteomalacia, multiple pathological fractures, deformities of the vertebral column with a decrease in growth, muscle hypotension, duck gait were noted. Other manifestations of chronic poisoning included anemia, persistent hypertensive syndrome, coronary artery disease, nephrotic syndrome. Many patients died from uremia.
Prolonged inhalation of cadmium-containing aerosols leads to chronic rhinitis and pharyngitis, anosmia, ulceration of the nasal septum. There is the formation of pulmonary fibrosis, chronic respiratory failure.
Acute Cd poisoning can end fatally due to acute renal failure and cardiopulmonary dysfunction. Cadmium nephropathy is accompanied by the development of chronic renal failure, leading to disability or death. Smokers, as well as people exposed to industrial exposure to cadmium, have a significantly increased risk of lung cancer and kidney cancer. It is possible to develop toxic cardiomyopathy, cadmium hepatitis, encephalopathy. It is reported that cadmium poisoning is associated with the occurrence of necrosis and tumors of the testicles, adenoma and prostate cancer in men.
Patients with signs of acute poisoning should be hospitalized in the ICU and consulted by a toxicologist. Further examination and treatment takes place with the participation of a nephrologist, pulmonologist, cardiologist. The patient’s professional and epidemiological history, the presence of nicotine addiction are being clarified. To confirm cadmium poisoning and assess its consequences,:
- Analysis for the content of trace elements. Due to the high nephrotoxicity of cadmium, it is preferable to determine its concentration in urine, but other biomaterial (blood, hair, nails) can also be used. Damage to the renal tubules is indicated by increased excretion of cadmium in combination with an increased content of beta-2 microglobulin in the urine.
- Assessment of renal function. For general urine analysis, the detection of glucosuria, proteinuria, microhematuria is specific, for general blood analysis ‒ hypochromic anemia. The biochemical complex includes the determination of the level of urea, creatinine, albumin, calcium, phosphorus, zinc serum.
- Biopsy. Taking into account the pronounced nephrotoxic effects of cadmium, kidney biopsies are resorted to to assess the degree of organ damage. It is also possible to determine the concentration of Cd in the nephrobioptate. Liver biopsy is performed less often.
- Radiation diagnostics. In acute inhalation poisoning, an X-ray of the lungs is performed. In case of chronic intoxication, accompanied by fragility and deformation of the skeleton, X-rays of tubular bones, spine, densitometry are performed. The complex of instrumental examinations also includes kidney ultrasound.
Cadmium nephropathy should be differentiated from nephropathies induced by other heavy metals (lead, mercury, copper, lithium). In addition, during the examination of patients, exclude:
- food toxicoinfection;
- pneumonitis of a different etiology;
- osteoporosis caused by other causes (hypovitaminosis D, endocrine disorders, alimentary calcium deficiency, etc.).
In all cases, with the established fact of cadmium intoxication, it is necessary to identify the source of poisoning (food, water, professional) and stop further contact with the compound. The subsequent tactics depend on the prescription and the way the toxic trace element enters the body:
- Detoxification. In acute food poisoning with cadmium, probe gastric lavage is performed, the patient is given antidotes, enterosorbents, saline laxatives. To accelerate the excretion of toxic substances through the kidneys, forced diuresis is carried out.
- Pharmacotherapy. The most effective is the use of chelators that ensure the excretion of cadmium in the urine. In acute inhalation pneumonitis, steroid hormones and diuretics are prescribed. In case of toxic liver damage, hepatoprotectors are recommended. Vitamin D, calcium and phosphorus supplements are used in the treatment of chronic cadmium.
- Substitution therapy. With signs of renal insufficiency, hemodialysis is indicated. With severe respiratory disorders, the patient is transferred to auxiliary ventilation or ventilator.
Prognosis and prevention
Chronic cadmium poisoning leads to permanent disability and disability due to irreversible damage to the kidneys, a decrease in respiratory reserves. Acute massive intake of the compound into the body or prolonged chronic intoxication can lead to death.
Prevention of cadmium poisoning involves quitting smoking, preventing the cultivation of crops on cadmium-containing soils, excluding contact with sources of trace elements in everyday life (nickel-cadmium batteries, etc.). In harmful industries, it is necessary to use PPE, observe safety precautions, undergo periodic medical examinations annually. The consumption of a sufficient amount of dietary fiber, pectin, protein, vitamins B6, C, D, minerals (copper, zinc, selenium, phosphates, calcium) will help to weaken the toxic effects of Cd.